Skip to main content
. 2011 Aug 22;108(36):14986–14991. doi: 10.1073/pnas.1109180108

Fig. 1.

Fig. 1.

Transcription function of AF2ER (L543A, L544A mutated ERα). (A) Schematic illustration of the ERα mutants. (B) HepG2 or HeLa cells were transfected with the reporter gene (3xERE-TATA-luc) and expression vectors for WT or mutated receptors were maintained with or without ligands. (C) HepG2 or HeLa cells were transfected with the reporter gene (7xAP1-TATA-luc) and expression vectors for WT or AF2ER. The cells were maintained with or without ligands. The luciferase activities for the each treatment were represented as fold change for the empty expression vector, pcDNA3 (no ERα). (D) Transrepression function of WT ERα and AF2ER. HeLa cells were transfected with the NF-κB reporter gene (3xMHC-luc), and expression vectors for p65/RelA and WT ERα or AF2ER were maintained with or without ligands. The luciferase activities were expressed relative to p65 activity in the absence of ligand (100%). (E) The effect of cofactors on ICI- or OHT-dependent AF2ER activation. HeLa cells were transfected with the 3xERE reporter gene and expression vectors for cofactors and AF2ER. The cells were maintained with or without ligands (100 nM E2, ICI, or OHT were used for treatments). Luciferase activity is represented as the mean ± SD of three independent experiments.